Explore the vast range of titles available.

This study evaluates the usefulness of serum KL-6, SP-D and TGF-β1 levels in assessing lung impairment and predicting interstitial lung disease (ILD) short-term progression in patients with interstitial pneumonia with autoimmune features (IPAF). A total of 24 patients with IPAF, 21 with connective tissue disease-associated ILD (CTD-ILD) and 23 with CTD without ILD were followed for 1 year. Serum levels of KL-6, SP-D and TGF-β1 were measured and their associations with disease severity and progression were analysed. KL-6, SP-D and TGF-β1 levels were significantly higher in IPAF and CTD-ILD patients compared to CTD without ILD (p < 0.0001, p = 0.0005 and p = 0.0001, respectively). KL-6 (r = 0.45, p = 0.002) and SP-D (r = 0.35, p = 0.02) levels correlated with lung involvement in HRCT in the ILD group. In IPAF, KL-6 levels correlated with pulmonary function tests (FVC%, TLCO%, and 6MWD) and SpO2, while SP-D correlated with 6MWD and SpO2. In CTD-ILD, KL-6 and SP-D levels were positively correlated with BAL cell count (KL-6: r = 0.58, p = 0.04; SP-D: r = 0.63, and p = 0.02). KL-6 also showed a negative correlation with the time since symptom onset (r = −0.51, p = 0.02). No significant associations were found between the baseline biomarker levels and ILD progression risk. KL-6 and SP-D may serve as potential biomarkers for assessing lung impairment in IPAF, though their predictive value for short-term prognosis remains uncertain.

Background Antiphospholipid antibodies (aPLs) are detected in 1–5% of the general population. They include lupus anticoagulant (LAC), anticardiolipin antibodies (aCL) and anti-β2-glycoprotein I antibodies (aβ2GPI). APL increases thrombotic risk, but the pathogenesis of this effect is not fully understood. Objectives The aim of this study was to evaluate oxidative and nitrosative stress biomarkers and their relation to certain rotational thromboelastometry (ROTEM) parameters as a risk factor for thrombosis in 32 patients in whom the presence of antiphospholipid antibodies was confirmed, but who had never experienced a thrombosis event (Group 1) in order to rule out any impact of thrombosis on stress parameters. The parameters were also assessed in a group of 23 healthy volunteers (Group 2). Methods To assess FRAP and thiol groups we used colorimetric method. The level of protein carbonylation, total pool of 3-nitrotyrosine in plasma proteins, 3-nitrotyrosine-containing fibrinogen as well as the acetyl-lysine-containing fibrinogen were estimated by ELISA. Lipid hydroperoxides were detected using the ferric-xylenol orange hydroperoxide assay. Additionally four ROTEM tests, i.e. INTEM, EXTEM, FIBTEM and APTEM, were performed. In statistical analysis the Mann-Whitney U-test, Student’s t-test and logistic regression were used. Results TBARS ( p  = 0,002), LOOH ( p  = 0,035) and carbonyl groups ( p  = 0,018) were markedly higher in Group 1 compared to Group 2. Also the acetyl-lysine-containing fibrinogen were significantly higher in Group 1 ( p  = 0,0028). Other biomarkers did not differ markedly between the studied groups. The obtained results of ROTEM, were not consistent and did not clearly indicate hypercoagulable state. Conclusion Study confirms increased levels of oxidative biomarkers in patients in whom the presence of antiphospholipid antibodies was confirmed, but who had never experienced a thrombosis event. Oxidative stress may an important role in the pathogenesis of APS and is not secondary to thrombosis.

Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is a common leukemia characterized by clonal expansion of mature CD5+/CD23 + B cells in the blood, bone marrow (BM) and lymphoid tissues. CLL can undergo extramedullary and extranodal infiltration, with one study noting an incidence of only 0.3 per 100,000 people, and in 17.6% of CLL patients in another report. The most common extranodal sites of leukemic involvement are the skin and central nervous system; however, other organs, including liver, lungs, kidney, gastrointestinal tract, bone, prostate and heart, are occasionally involved. The prognostic significance of extra-medullary CLL is still under debate, but the prognosis in such patients seems to be better in the era of novel targeted drugs. Following a diagnosis of extranodal CLL, survival appears to depend on the site of infiltration. This review presents an overview of CLL in patients with extramedullary and extranodal leukemic lesions, focusing on its epidemiology, pathogenesis, prognosis, clinical characteristics and treatment results.

Multiple myeloma (MM) is a genetically complex disease that results from a multistep transformation of normal to malignant plasma cells in the bone marrow. However, the molecular mechanisms responsible for the initiation and heterogeneous evolution of MM remain largely unknown. A fundamental step needed to understand the oncogenesis of MM and its response to therapy is the identification of driver mutations. The introduction of gene expression profiling (GEP) in MM is an important step in elucidating the molecular heterogeneity of MM and its clinical relevance. Since some mutations in myeloma occur in non-coding regions, studies based on the analysis of mRNA provide more comprehensive information on the oncogenic pathways and mechanisms relevant to MM biology. In this review, we discuss the role of gene expression profiling in understanding the biology of multiple myeloma together with the clinical manifestation of the disease, as well as its impact on treatment decisions and future directions.

Multiple myeloma (MM) is a hematological malignancy characterized by the clonal proliferation of plasma cells in the bone marrow (BM) microenvironment. Despite the progress made in treatment, some MM patients still die within the first year of diagnosis. Numerous studies investigating microRNA (miRNA) expression patterns suggest they may be good prognostic markers. The primary aim of this study was to analyze the expression of selected miRNAs in the serum of MM patients who were later treated with bortezomib-based regimens, and to determine their potential to predict early mortality. The study was conducted in 70 prospectively recruited patients with newly diagnosed MM admitted to the Department of Hematology of the Copernicus Memorial Hospital, Lodz (Poland) between 2017 and 2021. Among them, 17 patients experienced death within 12 months of diagnosis. The expression of 31 selected miRNAs was determined using a miRCURY LNA miRNA Custom PCR Panel. The obtained clinical data included patient characteristics on diagnosis, treatment regimen, response to treatment, and follow-up. Differential expression analysis found two miRNAs to be significantly downregulated in the early mortality group: hsa-miR-328-3p (fold change—FC: 0.72, p = 0.0342) and hsa-miR-409-3p (FC: 0.49, p = 0.0357). Univariate and multivariate logistic regression analyses were performed to assess the early mortality rate. The final model consisted of hsa-miR-409-3p, hsa-miR-328-3p, age, and R-ISS 3. It yielded an area under the curve (AUC) of 0.863 (95%CI: 0.761–0.965) with 88.2% sensitivity and 77.5% specificity. Further external validation of our model is needed to confirm its clinical value.

Over the past decade, chronic lymphocytic leukaemia (CLL) treatment has shifted from chemoimmunotherapy to targeted oral agents, predominantly Bruton’s tyrosine kinase inhibitors (BTKis) and the BCL-2 inhibitor venetoclax. These therapies have significantly improved outcomes and are now established as first-line treatment options. However, CLL remains incurable, and resistance or intolerance to both drug classes (double-refractory disease) is an emerging challenge. This has driven the development of novel therapeutic strategies, including non-covalent BTKis such as pirtobrutinib and nemtabrutinib, which retain activity in BTK C481-mutated disease. Next-generation BCL-2 inhibitors (sonrotoclax, lisaftoclax) and BTK degraders are promising in early clinical trials. Immunotherapeutic approaches, such as bispecific T-cell engagers, CD20/CD3 antibodies, and CAR-T cell therapies, provide additional options for high-risk patients. Although PI3K inhibitors remain under investigation, their role is yet to be defined due to safety concerns. Minimal residual disease (MRD)-guided, fixed-duration regimens represent a significant paradigm shift toward personalised treatment and potentially deeper remissions. Ongoing clinical studies are expected to introduce new effective therapies that may further transform the management of CLL in the coming years.

Introduction:Accelerated chronic lymphocytic leukemia (A-CLL) is a rare histological variant of CLL, which is associated with an aggressive clinical presentation and worse prognosis. The aim was to study the characteristics and treatment outcomes of A-CLL patients.Material and methods:The retrospective analysis included 106 A-CLL patients treated in Poland between 2013 and 2023.Results:Median overall survival (OS) for treatment-naive A-CLL was 6.05 years (95% CI: 4.7–NA) and median progression-free survival (PFS) was 5.66 years (95% CI: 4.05–6.34). Factors associated with worse PFS were: Eastern Cooperative Oncology Group > 2 (p < 0.0001) and del17p (p = 0.002). In the whole group, fludarabine-based regimens improved OS (p = 0.002) and PFS (p = 0.002). This therapy proved superior to R-CHOP-like protocols for both OS (p = 0.002) and PFS (p = 0.004). The difference in survival between fludarabine-based regimens and targeted therapy was not significant. However, the group of patients treated with new therapies was very heterogeneous. Fludarabine (p = 0.004) or targeted therapy (p = 0.02) in any line of treatment during acceleration was associated with a reduced risk of death.Conclusions:This study represents one of the largest datasets of A-CLL patients and shows its poorer prognosis compared to typical CLL. Chronic lymphocytic leukemia directed therapy should be considered as a treatment modality of choice for A-CLL. R-CHOP protocols are less effective.